<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bartolini E</submitter><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>963-72</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2258229</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>60(4)</volume><pubmed_abstract>While it is generally accepted that anaerobic metabolism is required during infection, supporting experimental data have only been described in a limited number of studies. To provide additional evidence on the role of anaerobic metabolism in bacterial pathogens while invading mammalian hosts, we analysed the effect of the inactivation of FNR, the major regulatory protein involved in the adaptation to oxygen restrictive conditions, and of two of the FNR-regulated genes on the survival of Neisseria meningitidis serogroup B (MenB) in vivo. We found that fnr deletion resulted in more than 1 log reduction in the meningococcal capacity to proliferate both in infant rats and in mice. To identify which of the FNR-regulated genes were responsible for this attenuated phenotype, we defined the FNR r</pubmed_abstract><journal>Molecular microbiology</journal><pubmed_title>Role of FNR and FNR-regulated, sugar fermentation genes in Neisseria meningitidis infection.</pubmed_title><pmcid>PMC2258229</pmcid><funding_grant_id>R01 AI046464</funding_grant_id><funding_grant_id>T32-HL007951</funding_grant_id><funding_grant_id>R01 AI046464-01A1</funding_grant_id><funding_grant_id>T32 HL007951</funding_grant_id><funding_grant_id>R01-AI46464</funding_grant_id><pubmed_authors>Shaik Y</pubmed_authors><pubmed_authors>Galli G</pubmed_authors><pubmed_authors>Welsch JA</pubmed_authors><pubmed_authors>Frigimelica E</pubmed_authors><pubmed_authors>Grandi G</pubmed_authors><pubmed_authors>Grifantini R</pubmed_authors><pubmed_authors>Giovinazzi S</pubmed_authors><pubmed_authors>Bartolini E</pubmed_authors><pubmed_authors>Genco C</pubmed_authors><pubmed_authors>Granoff DM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Role of FNR and FNR-regulated, sugar fermentation genes in Neisseria meningitidis infection.</name><description>While it is generally accepted that anaerobic metabolism is required during infection, supporting experimental data have only been described in a limited number of studies. To provide additional evidence on the role of anaerobic metabolism in bacterial pathogens while invading mammalian hosts, we analysed the effect of the inactivation of FNR, the major regulatory protein involved in the adaptation to oxygen restrictive conditions, and of two of the FNR-regulated genes on the survival of Neisseria meningitidis serogroup B (MenB) in vivo. We found that fnr deletion resulted in more than 1 log reduction in the meningococcal capacity to proliferate both in infant rats and in mice. To identify which of the FNR-regulated genes were responsible for this attenuated phenotype, we defined the FNR r</description><dates><release>2006-01-01T00:00:00Z</release><publication>2006 May</publication><modification>2025-04-04T08:58:50.145Z</modification><creation>2019-03-27T02:44:13Z</creation></dates><accession>S-EPMC2258229</accession><cross_references><pubmed>16677307</pubmed><doi>10.1111/j.1365-2958.2006.05163.x</doi></cross_references></HashMap>